{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T18:00:48Z","timestamp":1780077648271,"version":"3.54.0"},"reference-count":24,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[1999,1,19]]},"abstract":"<jats:p>\n            <jats:italic>Background<\/jats:italic>\n            \u2014Accumulating evidence suggests that the local synthesis of endothelin-1 (ET-1) plays a role in the development of heart failure in vivo. We investigated the role of endothelin-converting enzyme-1 (ECE-1), which mediates the conversion of big ET-1 to mature ET-1, in the development of \u03b1\n            <jats:sub>1<\/jats:sub>\n            -adrenergic\u2013stimulated hypertrophy in cultured neonatal rat cardiac myocytes.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Methods and Results<\/jats:italic>\n            \u2014Phenylephrine (PE) induced the expression of ET-1 in rat cardiac myocytes and accelerated the conversion of big ET-1 to ET-1. The\n            <jats:italic>ECE-1<\/jats:italic>\n            mRNA levels were markedly increased 3 hours after PE stimulation (3.6-fold compared with saline stimulation,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.005). A specific ECE-1 antagonist, FR901533, inhibited the PE-stimulated increase in protein synthesis rate by 45% (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.05). As genetic markers for the hypertrophic response, FR901533 inhibited the PE-stimulated transcriptional activities of the 3.5-kb\n            <jats:italic>\u03b2-myosin heavy chain<\/jats:italic>\n            promoter by 79% (\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01) but did not affect that of the 3.4-kb\n            <jats:italic>atrial natriuretic factor<\/jats:italic>\n            (\n            <jats:italic>ANF<\/jats:italic>\n            ) promoter. In Bio14.6 Syrian cardiomyopathic hamsters, ventricular ET-1 and\n            <jats:italic>ANF<\/jats:italic>\n            mRNA levels did not correlate at 2 different stages.\n          <\/jats:p>\n          <jats:p>\n            <jats:italic>Conclusions<\/jats:italic>\n            \u2014ET-1-independent pathways may mediate activation of the\n            <jats:italic>ANF<\/jats:italic>\n            gene program in ventricular myocytes both in vitro and in vivo. These results also indicate that the conversion of big ET-1 to ET-1 in rat cardiac myocytes is required for the development of \u03b1\n            <jats:sub>1<\/jats:sub>\n            -adrenergic-stimulated hypertrophy and\n            <jats:italic>\u03b2-myosin heavy chain<\/jats:italic>\n            gene transcription.\n          <\/jats:p>","DOI":"10.1161\/01.cir.99.2.292","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:42:29Z","timestamp":1339461749000},"page":"292-298","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":27,"title":["The Role of Endothelin-Converting Enzyme-1 in the Development of \u03b1\n            <sub>1<\/sub>\n            -Adrenergic-Stimulated Hypertrophy in Cultured Neonatal Rat Cardiac Myocytes"],"prefix":"10.1161","volume":"99","author":[{"given":"Satoshi","family":"Kaburagi","sequence":"first","affiliation":[{"name":"From the Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan; and the Department of Bioscience, National Cardiovascular Research Center, Osaka, Japan (T.S., T. Masaki)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Koji","family":"Hasegawa","sequence":"additional","affiliation":[{"name":"From the Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan; and the Department of Bioscience, National Cardiovascular Research Center, Osaka, Japan (T.S., T. Masaki)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatsuya","family":"Morimoto","sequence":"additional","affiliation":[{"name":"From the Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan; and the Department of Bioscience, National Cardiovascular Research Center, Osaka, Japan (T.S., T. Masaki)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Makoto","family":"Araki","sequence":"additional","affiliation":[{"name":"From the Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan; and the Department of Bioscience, National Cardiovascular Research Center, Osaka, Japan (T.S., T. Masaki)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tatsuya","family":"Sawamura","sequence":"additional","affiliation":[{"name":"From the Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan; and the Department of Bioscience, National Cardiovascular Research Center, Osaka, Japan (T.S., T. Masaki)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tomoh","family":"Masaki","sequence":"additional","affiliation":[{"name":"From the Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan; and the Department of Bioscience, National Cardiovascular Research Center, Osaka, Japan (T.S., T. Masaki)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shigetake","family":"Sasayama","sequence":"additional","affiliation":[{"name":"From the Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan; and the Department of Bioscience, National Cardiovascular Research Center, Osaka, Japan (T.S., T. Masaki)."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1038\/332411a0"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(17)32298-6"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1994.2343"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI116579"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.6.3221"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.93.11.2068"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(17)30538-0"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/384353a0"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.89.4.8149524"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.272.32.20049"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.88.2.8339400"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.27.2.259"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.94.11.2930"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.78.2.322"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/13.7.2485"},{"key":"e_1_3_2_16_2","first-page":"96","volume":"1997","year":"1997","unstructured":"Hasegawa K, Lee SJ, Jobe SM, Markham BE, Kitsis RN. cis-Acting sequences that mediate induction of \u03b2-myosin heavy chain gene expression during left ventricular hypertrophy due to aortic constriction. 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